lori and tom said:
Yes it makes sense to me that if the curve is flat than a 50 is no need for any urgency...but dear Illlka, a flat curve with a 50 midcycle is a time to try to wean kitty off juice no? I mean those would be a day in the greens.
Tom is just starting to flatten out on this 1 unit and today may be very telling as his pmps last night was lower 110 and his +11 this morning was 139 and he just ate so let's knock 30 points off that by amps....and i'll be around for some testing today.
The one thing you know i hate is when i have to spend the day standing guard while Tom is flirting with the 30's...kwim?
Yes, I kwym
.. no one wants to stand guard.
Is a flat curve with a 50 midcycle time to wean the kitty off the juice? yes and no. And if yes,
how do we do that? Three ways that can all work: hold, decrease, raise.
1) Lowering the dose is the most frequent choice, though not necessarily the best choice. I am always in favor of decreasing if I think it will work -- and yes, sometimes you have to try to know. It is often not my first choice because it might appear to work at first, but you might be tapping into the kitty's bank to pay for the missing insulin, and you won't know that until the bank account gets low and you start getting some yellow and pink slips from accounting
Typically these appear in 2-5 cycles after the decrease, but sometimes it takes 20 cycles or more, and by that time plenty of damage has been done because the shed has been depleted in a real way. However,
if the kitty is really strong by this time, decrease can work and can open the door toward remission, and it is lovely to see. The risk is that we are betting on a state of health and readiness which, if it is not truly established, will backfire. There are many many charts where you can see cats that were on .5u or even less for long periods and now are on more than 1u -- and if you look back to what happened, you often see a pattern of unsuccessful attempts to coax the cat down by decreasing before it is ready to get with the program.
2) Raising -- this works only if you are
increasing in order to be able to decrease, if the curve is flat and the cat needs a little extra experience in really low ranges, or if a stubborn "hold" in the middle ranges needs to be shocked out of the cat's system. The risks of raising if there is any agitation in the curve are too obvious to need commenting.
3) If you
hold and extend the kitty's experience of 40 to 99 glucose levels, which is my favorite approach (except you can't maintain for too long) the cat will rewrite the system "memory" and may start to go lower by himself. Why does that happen? it is because the "exogenous" insulin amount he needs at that stage is no longer a fixed quantity, like .X units -- you are not making up for a physical shortfall but instead you are correcting a systemic
perception: the insulin you inject is a systemic message, which can be reduced as his own systems begin to support the glucose at the healthy range. When the curve is flat and low it means that there are no competing system memories which produce the snap-back to a higher level, which is (mistakenly, in my view) called "bounce" (or "panicky liver," equally fictitious because the liver makes no decisions but only opens the storehouse if the right molecular key is in the lock).
The coherent view behind this analysis of all three strategies is part of a major revolution in medicine, happening before our eyes, broadly known (or partly known) as the "systems biology" view (ref Dr. Leroy Hood, the immunologist who invented the DNA sequencer, and Craig Venter, who sequenced the human genome and views DNA as a computer). It is based on a kind of conditional equivalence or interchangeability of the physical and the virtual. That is to say, in the case of diabetes, when the cat is hyperglycemic, it is only partly a case that it is caused by lack of insulin or by pancreatic damage -- or rather, to focus on the lack of insulin, which is a fact, is an
incomplete view of the disease; it is really that the cat, for reasons not fully understood but which go to the root of its biological intelligence, has entered a system state where it either (a) does not produce insulin though it can, or (b) is not able to bind the insulin to the receptors on the molecular level, and what's more startling, both of these states are responses to system chemical messages which do not originate in pancreatic damage, though they can cause it. So what is really going on? Well, in effect, because of the disease, the internal endocrine system
acquires a pathological norm, a parasitic homeostatic state called diabetes which the cat thinks is the "ok state" and to which it snaps back if you correct it with insulin. It is a software problem that causes a hardware problem, and in the case of Type 2 diabetes, at least, can uncause it. Thus the systems view (the diabetes as a corrupt
memory) reveals a disorder involving the cooperation of all the other endocrine players -- glucagon, liver response, etc. Hyperglycemia corrupts or deletes the healthy systemic hormonal registers, and over-writes them with the pathological one that supports diabetes as if it were normal.
Just some more thoughts..
